533119
research-article2014

HSBXXX10.1177/0022146514533119Journal of Health and Social BehaviorPridemore

Incarceration and Health

The Mortality Penalty of
Incarceration: Evidence from a
Population-based Case-control
Study of Working-age Males

Journal of Health and Social Behavior
2014, Vol. 55(2) 215­–233
© American Sociological Association 2014
DOI: 10.1177/0022146514533119
jhsb.sagepub.com

William Alex Pridemore1

Abstract
There is a growing body of research on the effects of incarceration on health, though there are few
studies in the sociological literature of the association between incarceration and premature mortality.
This study examined the risk of male premature mortality associated with incarceration. Data came from
the Izhevsk (Russia) Family Study, a large-scale population-based case-control design. Cases (n = 1,750)
were male deaths aged 25 to 54 in Izhevsk between October 2003 and October 2005. Controls (n = 1,750)
were selected at random from a city population register. The key independent variable was lifetime
prevalence of incarceration. I used logistic regression to estimate mortality odds ratios, controlling for
age, hazardous drinking, smoking status, marital status, and education. Seventeen percent of cases and
5 percent of controls had been incarcerated. Men who had been incarcerated were more than twice as
likely as those who had not to experience premature mortality (odds ratio = 2.2, 95 percent confidence
interval: 1.6–3.0). Relative to cases with no prior incarceration, cases who had been incarcerated were
more likely to die from infectious diseases, respiratory diseases, non–alcohol-related accidental poisonings,
and homicide. Taken together with other recent research, these results from a rigorous case-control
design reveal not only that incarceration has durable effects on illness, but that its consequences extend
to a greater risk of early death. I draw on the sociology of health literature on exposure, stress, and social
integration to speculate about the reasons for this mortality penalty of incarceration.

Keywords
case-control study, health, incarceration, premature mortality, Russia
Incarceration rates in the geopolitical powers of the
United States and Russia are among the highest in
the world.1 The rapid expansion of the U.S. penal
system began in earnest in the 1970s, while largescale imprisonment in Russia dates back further.
Although their reasons for resorting to mass incarceration vary, one critical outcome is that both
nations imprison a large number of their citizens—730 and 519 per 100,000 residents in the
United States and Russia, respectively (International
Centre for Prison Studies 2012)—without efficient
concomitant structures to reintegrate inmates back
into society or to mitigate the impact of incarceration on other negative outcomes. This has led

to substantial research in the United States on the
collateral consequences of mass imprisonment for
individuals, communities, and society. Studies have
examined imprisonment as a barrier to future marriage and employment (Huebner 2005; Pager 2003),
its negative effect on already disadvantaged communities (Clear 2007), its role in ethnic and class
1

Georgia State University, Atlanta, GA, USA

Corresponding Author:
William Alex Pridemore, Department of Criminal
Justice and Criminology, Georgia State University, 1213
Urban Life Building, Atlanta, GA, 30302, USA.
E-mail: wpridemore@gsu.edu

216	
inequality (Pettit and Western 2004; Western 2002),
and its influence on the outcomes of senatorial and
presidential elections (Uggen and Manza 2002).
Medical sociology largely ignored the potential
health effects of imprisonment until recently,
though a growing literature has begun to address
the topic (Patterson 2010; Wildeman 2012), including studies published in this journal (Massoglia
2008a; Schnittker and John 2007; Schnittker,
Massoglia, and Uggen 2012; Turney, Wildeman,
and Schnittker 2012). Incarceration may negatively
influence health via multiple mechanisms. First,
incarceration increases exposure to and the likelihood of contracting infectious diseases like HIV,
hepatitis C, and tuberculosis (Johnson and Raphael
2009; Massoglia 2008a; Stuckler et al. 2008).
Second, major life events (Thoits 1995) and primary and secondary stressors (Pearlin 1989) can
create enduring negative health outcomes.
Imprisonment certainly constitutes such an event,
as it exposes one to the initial shock of incarceration, the acute stress of the prison environment, and
the chronic stress associated with marginalization
in multiple domains of life following release.
Medical research shows that stress sustained over a
long period can have detrimental physiological
effects, compromise the immune system, and lead
to long-term health problems. Third, incarceration
disrupts social ties to spouses and children and to
employment and education opportunities that
might otherwise provide protective effects against
negative health outcomes. Recent studies demonstrate the short- and long-term health effects of
incarceration resulting from exposure, stress, and
stigma (Fazel and Baillargeon 2011; Massoglia
2008a, 2008b; Schnittker and John 2007).
In spite of the increasing interest in the health
effects of imprisonment, the individual-level
impact of incarceration on the most serious health
outcome, mortality, remains absent from the sociological literature (see Wildeman 2012 for a recent
population-level study). While there is detailed
information on the distribution and causes of death
while incarcerated (Mumola 2007) and on the
impact of incarceration on mortality while imprisoned (Patterson 2010), only a few studies address
the enduring effects of incarceration on premature
mortality upon release from prison (Binswanger et
al. 2007; Rosen, Schoenbach, and Wohl 2008;
Spaulding et al. 2011). However, these studies usually (1) control only for age, sex, race, and perhaps
a simple education variable dichotomized on
receipt of a high school diploma and (2) address
only briefly the theoretical mechanisms that may

Journal of Health and Social Behavior 55(2)
link incarceration to early death. In this study, I
used a case-control design to determine the risk of
premature mortality among working-age males
associated with incarceration, controlling for the
known determinants of premature mortality in this
sample, including detailed measures of hazardous
drinking, smoking status, marital status, and education. Results suggest a substantial mortality penalty
of incarceration, and I draw on the literatures on
exposure, stress, and social integration to explain
the association.

Background
There are several reasons incarceration may be
associated with negative health outcomes, including premature mortality. Incarceration increases
exposure to infectious diseases and subjects one to
the prolonged stress of the prison environment. The
stress of prison life dissipates upon release, but in
the struggle to reintegrate into society the felon and
former inmate is faced with a series of new challenges that create their own stress. In addition, both
during and following incarceration, one’s ties to
important protective social bonds and networks
like family and employment are threatened or cut
off. Each of these factors—exposure to disease,
stress, and disruption of social bonds—is associated with negative health outcomes and premature
mortality.2

Incarceration and Exposure to
Infectious Diseases
Prisons house populations with generally poor
health and a high rate of infectious disease. The
most common life-threatening infectious diseases
in correctional facilities are tuberculosis (TB), hepatitis, and HIV. Sexually transmitted infections and
methicillin-resistant staphylococcus aureus are
also common (Bureau of Justice Statistics 2008;
National Commission on Correctional Health Care
2002). About 10 percent of male inmates in U.S.
state prisons have confirmed tuberculosis, about
5 percent have confirmed hepatitis, and about
1.5 percent of inmates in state and federal prisons
are HIV-positive (Bureau of Justice Statistics 2008,
2009). The prevalence of each is underenumerated,
however, with true infection rates likely much
higher. Inmates are not only disproportionately
exposed to infectious diseases, but exposure occurs
in an environment where group quarters and prison
culture create efficient conditions for disease transmission, including overcrowding, poor health care,

Pridemore	
poor nutrition, and a host of risky behaviors like
sharing hygienic facilities and personal hygiene
items, amateur tattooing and piercing, practicing
unprotected sex, and using unsterilized drug injection equipment.
It is impossible to know for sure what proportion of ex-inmates with an infectious disease contracted their illness while in prison. There is little
doubt, however, that the prison is an especially
important setting for TB: increasing incarceration
rates in several nations are associated not only with
a greater number of TB infections among inmates
and ex-inmates but also with growing TB infection
rates among their general populations (Stuckler
et al. 2008). Similarly, U.S. prisons are seen as a
primary engine driving the non-institutionalized
population’s exposure to hepatitis C as infected
inmates are released. In a study of imprisonment
and infectious disease, Massoglia (2008a) found
that those previously incarcerated were about four
times more likely than those not previously incarcerated to self-report urinary tract infections, hepatitis, and tuberculosis. Johnson and Raphael (2009)
found that changes in black incarceration rates
between 1982 and 1996 were nearly entirely
responsible for the black-white disparity in AIDS
infection rates during this period.

Incarceration, Stress, and Health in
Prison and Following Release
Massoglia (2008a) draws on the medical sociology
literature to explain how incarceration can create
negative health outcomes. He argues that the shock
of incarceration as a major life event, the stressful
immediate conditions of imprisonment, and the
long-term extralegal consequences of incarceration
following release lead to a greater prevalence of
stress-related illnesses among former inmates.
Incarceration is both an acute and an enduring
stressor. The initial shock of imprisonment is a
traumatic event on par with marital separation and
the death of a close family member (Holmes and
Rahe 1967). Major life events that precipitate dramatic change in a short time period can create substantial stress and lead to detrimental health effects
(Thoits 1995; Wheaton 1994). However, as Pearlin
(1989) notes, it is important not to confuse what
may seem like discrete events with more enduring
stressors, of which he cites incarceration as one
example. One element of incarceration’s enduring
nature is that it is not an isolated event but can last
for years, thereby presenting chronic stress on top
of the initial shock. The proximate sources of stress

217
in prison are manifold and constant; they include
lack of privacy, overcrowded conditions, antagonistic relationships with guards and fellow inmates,
witnessing violence, and the threat of violent
victimization.
Another element of the enduring impact of
imprisonment is that even upon release, former
inmates face stressful consequences of prison life
that have health effects. I discuss some of these in
the next section on the disruption of social bonds
and networks. In short, these ongoing consequences of incarceration—social stigma, poor
employment prospects, decreased earnings, family
problems, the inability to participate fully in society, lack of control over important aspects of one’s
life—are secondary stressors and durable strains
(Pearlin 1989) that not only are problematic in
themselves but also negatively influence health
(Massoglia 2008a; Schnittker and John 2007).
There is substantial evidence from the psychoneuroimmunology literature that chronic stress is
associated with immune dysfunction (Glaser and
Kiecolt-Glaser 2005). Psychological stress occurs
when environmental conditions exceed the individual’s coping ability, producing distress, anxiety,
and negative thoughts, emotions, and moods. The
central nervous, endocrine, and immune systems
interact with each other in complex ways, and
stressors can disrupt their function and weaken
immune response. Chronic stressors are especially
detrimental and can result in negative health effects
by increasing susceptibility to and the severity of
infectious diseases. Examples of continuous stressors that have been shown to alter immune functions
include isolation and exposure to hostile conditions, both of which are characteristics of imprisonment, and the resulting immunological dysfunction
can last for extended periods (Glaser and KiecoltGlaser 2005). Stress-induced immune dysfunction
perversely increases the inmate’s vulnerability at
precisely the time when exposure to infectious diseases is greatest, that is, during imprisonment. Of
course, the health effects of contracting an infectious disease while incarcerated persist upon
release from prison.
While the evidence is weaker, there is some
suggestion that chronic stress may also be associated with cardiovascular disease (Dimsdale 2008).
Incarceration is a chronic stressor in itself, and the
hypertension resulting from stress can persist far
beyond the duration of the initial stressor. Since
different types of stressors—again, of the type
often examined in studies of stress and cardiovascular disease like those associated with jobs,

218	
relationships, and feelings of unfair treatment and
discrimination (Krieger and Sidney 1996)—continue following release from prison, the former
inmate remains at risk of premature mortality long
after release from prison.
Massoglia (2008a) found that relative to those
who had not been incarcerated, those who had were
at greater risk of being medically diagnosed with
stress-related illnesses like psychological problems, hypertension, heart disease, and chronic lung
disease. They were also at a greater risk of selfreporting stress-related conditions like chest pain,
depression, and general health problems. Schnittker
and John (2007) also found significant long-term
health effects of imprisonment following release.
Consistent with the argument that these effects are
stress related, Schnittker and John’s results provided considerable evidence that the effects were
due less to incarceration itself and more to the
enduring stigma associated with it. Similarly,
Schnittker et al. (2012) and Turney et al. (2012)
both found incarceration to be associated with
mental health, including major depression and
other serious psychiatric disorders.

Incarceration, Disruption of Social
Integration, and Health Effects
Social bonds, networks, support, and capital provide important protective effects against negative
health outcomes. From a life course perspective,
incarceration is a major turning point and a remarkably disruptive force against social integration
(Sampson and Laub 1993; Western 2002). It has
corrosive effects on employment, marriage, and
other forms of social integration that are otherwise
protective of health. The effects of incarceration on
labor market opportunities are considerable, diminishing the chances of both employment and earnings. There is substantial evidence of an association
between incarceration and subsequent employment, and experimental research reveals that
employers are reluctant to hire former inmates
(Pager 2003). This effect extends to wages, with
prior imprisonment restricting access to careeroriented occupations and often leaving ex-inmates
stuck in poor jobs. This cuts off the potential for
earnings growth over the employment career
(Sampson and Laub 1993) and results in a wage
penalty of 10 percent to 30 percent for ex-inmates
(Western, Kling, and Weiman 2001). Western
(2002) found that the individual-level effect on
wage mobility is so strong and imprisonment so
widespread among young black men in the United

Journal of Health and Social Behavior 55(2)
States that incarceration plays a key role in ethnic
wage inequality at the aggregate level. Finally, a
simple yet often overlooked fact is that ex-inmates’
employment opportunities are often limited to jobs
that do not provide health insurance.
Incarceration has negative effects on maintaining stable relationships.3 Being in prison imposes a
separation—exacerbated because inmates are often
institutionalized far from home—that makes it difficult to maintain the friendship and trust required
of a stable relationship (Nurse 2002). Similarly, the
social and psychological adaptations required for
life in prison are not easily discarded upon release,
making it difficult to reintegrate and to maintain
healthy relationships with family and friends
(Braman 2004). Following release, the stigma of
incarceration and the inability to provide for one’s
family due to the employment effects of prison
make an ex-inmate less desirable as a mate (Wilson
1987). These effects are manifested in lower marriage and higher divorce rates among formerly
incarcerated men (Huebner 2005; Western 2006).
The past two decades have produced a voluminous literature on the individual and social determinants of health and health inequalities. This literature
shows that the relationships with health of employment and marital status are complex, and both relationships are bidirectional. Nevertheless, this
literature also clearly shows that employment,
income, and the strength of family ties are associated
with morbidity and mortality, as are social capital and
social support. Ross and Mirowsky (1995) showed
that full-time employment slowed declines in perceived health and physical functioning, and studies of
the United States (Backlund, Sorlie, and Johnson
1996) and Europe (Ecob and Davey Smith 1999)
revealed relationships between income and morbidity
and mortality. An analysis of the same case-control
data employed in the present study found inverse relationships with premature mortality for both education
(as a measure of socioeconomic status) and marriage
(Pridemore et al. 2010). The protective effect of marriage against morbidity and mortality, especially for
men, is a common finding and has been for decades
(Verbrugge 1979).

Individual-level Studies of Incarceration
and Mortality
A few studies have examined the association between
incarceration and mortality. Most of these studies
looked at the effects in the period immediately following release from prison, which is an especially
risky time for former inmates. A retrospective cohort

Pridemore	
study by Binswanger et al. (2007) of all inmates
released from the Washington State Department of
Corrections between 1999 and 2003 linked prison
records to the National Death Index, comparing mortality rates of the previously incarcerated with the
state population. With a mean follow-up period of
about two years, they found that those who had been
incarcerated were more than three times more likely
to die than other residents in the same region.
European studies in Scotland (Seaman, Brettle, and
Gore 1998) and France (Verger et al. 2003) also found
an increased risk of mortality soon after release from
prison. Lim et al. (2012) found similar results for
those released from New York City jails.
A few studies have looked at the long-term
effects of incarceration on mortality. Relative to
injuries and other external causes of death that
were the focus of studies with shorter follow-up
periods, these studies allow the authors to examine
the impact of incarceration on deaths due to internal and chronic causes. Rosen et al. (2008) compared the mortality of ex-inmates to other state
residents, linking prison records to state death
records from North Carolina from 1980 to 2005.
They found that ex-prisoners were significantly
more likely to experience early death. Spaulding et
al. (2011) carried out a cohort study of all persons
incarcerated in Georgia state prisons on June 30,
1991. They linked prison and mortality records to
determine 15.5-year survival, finding high standardized mortality rates for those who had been
released from prison.

Data and Methods
Study Design and Population
This was a large-scale population-based case-control
study. It was large scale in both practical and formal
terms. Practically, the original project and the present
analysis were (1) undertaken by institutions and
researchers in multiple countries including Russia,
Germany, the United Kingdom, and the United States
and (2) scholars from multiple disciplines including
epidemiology, demography, medicine, and sociology
and (3) involved multiple local agencies like the
police, narcology clinics, and the vital registration
system. It was also large scale in more formal methodological terms: A prior research project in the city
acted as a de facto pilot study for the current project, a
team of over 30 people interviewed more than 3,500
case and control proxies, the research team collected
forensic autopsy data on decedent cases, and measurement research was undertaken to determine

219
which types of questions were more reliable when
using proxy respondents.
A study is population based if the cases come
from a precisely defined and identified population
and the controls are sampled directly from this
population. The most desirable alternative for a
population-based case-control study is to sample
controls randomly, which was feasible in this study
because a population register was available for
Izhevsk. As opposed to disease-based research
undertaken to treat or cure a specific disease, population-based research refers to human subjects
research where the objective is to measure, determine the causes of, and improve the health of populations. This was also the case with the larger
project carried out here, as the mission was to
address the mortality crisis in the population.
A case-control study is an observational study
in which two existing groups that differ on some
outcome are identified and compared. This design
is usually employed to identify factors that contribute to some condition. In this case, that condition
was premature mortality. The potential relationship
of the suspected risk factor—in this case incarceration—is examined by comparing the cases and
controls with regard to how frequently exposure is
present in each group. The use of case-control
designs are rare in sociological analyses.
Data for this analysis were collected as part of
the Izhevsk Family Study (IFS), which was
designed to examine premature mortality among
working-age Russian males (Leon et al. 2007;
Tomkins et al. 2007). Human subjects and ethical
approvals for the study were obtained from the
committees of the Izhevsk Medical Academy and
the London School of Hygiene and Tropical
Medicine. Izhevsk is an industrial city on the
western side of the Ural Mountains. Prior research
in the region revealed the feasibility of carrying
out such a complex investigation in this location
(e.g., Shkolnikov, Meslé, and Leon 2001). Izhevsk
had a population of about 630,000 residents in
2002 according to the Russian Census carried out
that year. It is a typical Russian industrial city, and
residents had both an average life expectancy and
a distribution of deaths by cause in working-age
men that was very similar to that of Russia as a
whole. Russia rivals the United States in its incarceration rate, ensuring a high enough lifetime
prevalence of incarceration for meaningful analysis given the number of cases and controls in the
study.
Cases were deceased men aged 25 to 54 years
who died from any cause between October 20,

220	
2003, and October 3, 2005, and who were living in
an Izhevsk household with at least one other person
at the time of death. The upper age range was purposely truncated at 55 years because the IFS was
designed to examine premature mortality (and life
expectancy of Russian males was about 60 years).
The IFS team was notified of deaths by the registrar of deaths. Cause of death was coded using the
10th Revision of the International Classification of
Diseases. Of the 1,750 cases with a proxy interview, cause of death was established in 72 percent
of the cases by forensic autopsy, in 11 percent by a
non-forensic pathologist, in 11 percent by a doctor
who had treated the decedent, and in 5 percent by a
doctor who had not treated the decedent. There
were no significant differences in the distribution
of causes of death between cases for which a proxy
interview was obtained and those for which a proxy
interview was not obtained (Leon et al. 2007:2003,
Figure 1). Controls were living men selected from
a 2002 population register and who were living in
an Izhevsk household with at least one other person. Each month new controls were randomly
selected from within five-year age bands from the
sampling frame, such that the control sample with
proxy interviews reflected the same ages as the
accumulating series of cases with proxy interviews.
This sample selection process yielded 1,750 cases
and 1,750 controls.
A team of 34 trained interviewers used a structured questionnaire to obtain information about
cases and controls from proxy respondents living
in the same household. Oral consent was obtained
from proxy informants. Nearly all case proxy interviews took place six to eight weeks after death.
Proxy interviews were done between December 11,
2003, and November 16, 2005. Case and control
proxy interviews were carried out at the same rate
throughout the data accumulation period. Interviewers returned to an address up to three times to
get a response. When more than one proxy was
available, a prespecified priority order was used,
with wives or partners being the first choice. Most
proxy interviews were with wives or partners (59
percent for cases, 85 percent for controls), followed by mothers (21 percent for cases, 9 percent
for controls). Other less common informants
included adult offspring, siblings, fathers, or other
relatives. For validation purposes, the research
team obtained proxy interviews from two informants living in the same household in a subset of
200 cases and 200 controls. The interviews with
proxies took place in private to avoid contamination of responses. The questionnaire covered a

Journal of Health and Social Behavior 55(2)
wide range of topics, including alcohol consumption, smoking, and social, economic, and demographic information. Most questions were derived
from established and validated instruments, and in
most cases the reference period for the surveyed
behaviors and experiences was the prior 12 months.

Measures
The main independent variable in the present study
was lifetime prevalence of incarceration of any sort
for any length of time. The question on the instrument asked: “Had he [i.e., the decedent or the control] ever been in any kind of prison?” Response
categories included: “yes, in the previous year”;
“yes, between 1 and 5 years ago”; “yes, more than
5 years ago”; “no, never”; “difficult to answer”;
and “refuse to answer.” For the purposes of this
analysis, I created a dichotomous variable for lifetime prevalence and a separate categorical variable
in which no/never was the reference group, with
yes in the prior year, yes 1 to 5 years ago, and yes
more than 5 years ago as the other categories.
I included controls for age group and for the
known determinants of premature mortality among
this group (Leon et al. 2007; Pridemore et al. 2010),
including smoking status, marital status, education,
and hazardous drinking. Age was included as seven
five-year age categories: 25–29, 30–34, 35–39,
40–44, 45–49, 50–54, and 55+ (the latter contained
only one case and 11 controls). Smoking status
consisted of three categories: non-smokers, exsmokers, and current smokers. Marital status consisted of five categories: living together in a
registered marriage, living together in an unregistered marriage, never married, divorced/separated,
and widowed. Educational status consisted of six
categories: complete higher education, incomplete
higher, specialized secondary, complete secondary,
professional, and incomplete secondary. The “specialized” and “professional” categories may be
unfamiliar to Western readers; more information
can be found in Pridemore et al. (2010). Hazardous
drinking was a dichotomous variable coded 1 if
during the previous 12 months the person had gone
on a drinking binge of at least two days and/or at
least twice per week had an occurrence of drunkenness or a hangover or went to sleep with his clothes
on due to drinking. The type of drinking binge
mentioned here is known as zapoi in Russian and is
defined as going on a spree of continuous drunkenness lasting at least two days during which the person is completely removed from normal social life.
At the design stage of the IFS, a systematic review

221

Pridemore	
(Tomkins 2006) of the validity of proxy informant
data related to alcohol consumption led to the key
conclusion that the validity of proxy responses was
improved if questions were restricted to behaviors
that were directly observable. Further, subsequent
analyses (Leon et al. 2007) revealed problem
drinking as defined here was a strong determinant
of mortality among this population, with over
40 percent of all premature deaths among this
group shown to be attributable to a similar measure
of hazardous drinking.

Analysis
I used logistic regression to estimate mortality odds
ratios (ORs) comparing cases to living controls. I
estimated two models: the first was for lifetime
prevalence of incarceration; the second was for
how long before the interview (if ever) incarceration occurred. All ORs were adjusted for the controls described previously. Given the results of
model estimation, I compared the distributions of
causes of death for cases ever incarcerated relative
to cases never incarcerated.

Results
Table 1 shows the distribution of all variables
among the cases and controls. As revealed elsewhere (e.g., Leon et al. 2007; Pridemore et al.
2010), there are differentials in premature mortality
among this group based on hazardous drinking,
smoking status, marital status, and education. Table
1 suggests there may also be significant differences
between cases and controls in their experience with
incarceration. While only about 5 percent of controls were ever incarcerated, around 17 percent of
cases had been incarcerated. One percent of cases
and 0.1 percent of controls had been incarcerated in
the past year, 3.4 percent of cases and 1.0 percent
of controls had been incarcerated between one and
five years prior to the proxy interviews, and 12.3 percent of cases and 3.7 percent of controls had been
incarcerated at some point at least five years prior
to the proxy interviews.
Table 2 shows the mortality odds ratios for the
association between incarceration and premature
mortality, mutually adjusted for age, hazardous
drinking, smoking status, marital status, and education. As expected, problem drinking, smoking status, marital status, and education were all associated
with premature male mortality in this sample.
Model 1 shows the association of premature mortality with lifetime prevalence of incarceration. Net

of the control variables, males who had been incarcerated were more than twice as likely to experience premature mortality compared to males who
had never been incarcerated (OR = 2.2, CI: 1.6–
3.0). For Model 2, caution should be taken when
interpreting the results for time since incarceration
as the cells for incarceration during the last year
contain very small counts. Nevertheless, it is interesting to note the substantially heightened risk of
premature mortality for those who had been incarcerated in the 12 months prior to the proxy interview (OR = 11.8, CI: 1.5–92.5). The mortality odds
ratios for incarcerated 1–5 years prior (OR = 2.0,
CI: 1.1–3.8) and more than 5 years prior (OR = 2.1,
CI: 1.5–2.9) were essentially the same as each
other and the same as the mortality odds ratio for
lifetime prevalence of incarceration shown in
Model 1.
Finally, Table 3 provides the age-adjusted odds
of specific causes of death by lifetime prevalence
of incarceration. The comparison category no longer consists of the original controls, but instead of
decedent cases who had never been incarcerated.
ORs are presented in terms of those ever incarcerated relative to those never incarcerated. Table 3
shows that relative to cases who had never experienced incarceration, those who had been incarcerated were significantly more likely to have died
from respiratory diseases (OR = 1.79, CI: 1.19–
2.71), infectious diseases (OR = 3.10, CI: 1.74–
5.50), accidental poisonings that were not from
alcohol (usually drug overdoses; OR = 2.32, CI:
1.11–4.87), and homicide (OR = 1.99, CI:
1.04–3.82).4
In summary, the findings revealed that males
who had ever been incarcerated were more than
twice as likely to die prematurely, that this risk of
death was heightened further by incarceration
within the past year, and that decedents who had
been incarcerated were more likely than other
decedents to die from infectious and respiratory
diseases, drug overdoses, and homicide.

Discussion
More than 10 million people are imprisoned worldwide, with nearly 2.5 million incarcerated in the
United States alone (Walmsley 2009). While the
United States and Russia already resort to mass
imprisonment, the incarceration rate in two-thirds of
the world’s nations has increased in recent years
(Walmsley 2009). Since 95 percent of all prisoners
will eventually be released, the number of former
inmates is large and will continue to grow. Estimates

222	

Journal of Health and Social Behavior 55(2)

Table 1.  Distribution of Variables among Cases and Controls (n = 3,500).
Cases
 
Ever incarcerated
 No
 Yes
 Missing
When incarcerated
 Never
  In last year
  1–5 years ago
  >5 years ago
 Missing
Age group
 25–29
 30–34
 35–39
 40–44
 45–50
 50–54
 55+
Problem drinker
 No
 Yes
 Missing
Smoking status
 Non-smoker
 Ex-smoker
  Current smoker
 Missing
Marital status
  Married (registered)
  Married (unregistered)
 Never married
  Divorced or separated
 Widowed
 Missing
Education
  Complete higher
  Incomplete higher
  Specialized secondary
  Complete secondary
 Professional
  Incomplete secondary
 Missing

Controls

Total

(n = 1,750) Percentage (n = 1,750) Percentage (n = 3,500) Percentage
1,449
292
9

82.8
16.7
.5

1,662
83
5

95.0
4.7
.3

3,111
375
14

88.8
10.7
.4

1,449
17
60
215
9

82.8
1.0
3.4
12.3
.5

1,662
1
17
65
5

95.0
.1
1.0
3.7
.3

3,111
18
77
280
14

88.8
.5
2.2
8.0
.4

131
144
136
306
441
591
1

7.5
8.2
7.8
17.5
25.2
33.8
.1

130
145
145
293
429
597
11

7.4
8.3
8.3
16.7
24.5
34.1
.6

261
289
281
599
870
1,188
12

7.5
8.3
8.0
17.1
24.9
33.9
.3

679
917
154

38.8
52.4
8.8

1,223
309
218

69.9
17.7
12.5

1,902
1,226
372

54.3
35.0
10.6

133
149
1,468
—

7.6
8.5
83.9
—

373
218
1,158
1

21.3
12.5
66.2
.1

506
367
2,626
1

14.5
10.5
75.0
.0

930
205
215
342
57
1

53.1
11.7
12.3
19.5
3.3
.1

1,351
174
104
106
15
—

77.2
9.9
5.9
6.1
0.9
—

2,281
379
319
448
72
1

65.2
10.8
9.1
12.8
2.1
.0

135
36
340
560
442
209
28

7.7
2.1
19.4
32.0
25.3
11.9
1.6

354
43
405
535
299
100
14

20.2
2.5
23.1
30.6
17.1
5.7
.8

489
79
745
1095
741
309
42

14.0
2.3
21.3
31.3
21.2
8.8
1.2

suggest nearly 3 percent of U.S. adults and 5 percent
of adult males have spent time in a state or federal
prison (Bonczar 2003). Similarly, nearly 5 percent of

this sample of Russian males aged 25 to 54 had been
incarcerated in their lifetime.5 The large number of
people ever incarcerated in nations that rely heavily

223

Pridemore	

Table 2.  Mortality Odds Ratios for the Association between Premature Mortality from All Causes and
Measures of Incarceration (n = 3,085).

 
Ever incarcerated
 No
 Yes
When incarcerated
 Never
  In last year
  1–5 years ago
  >5 years ago
Age group
 25–29
 30–34
 35–39
 40–44
 45–50
 50–54
 55+
Problem drinker
 No
 Yes
Smoking status
 Non-smoker
 Ex-smoker
  Current smoker
Marital status
  Married (registered)
  Married (unregistered)
 Never married
  Divorced or separated
 Widowed
Education
  Complete higher
  Incomplete higher
  Specialized secondary
  Complete secondary
 Professional
  Incomplete secondary

Model 1: Ever Incarcerated

Model 2: When Incarcerated

OR (95 percent CI)

OR (95 percent CI)

1.0 [reference]
2.2 (1.6–3.0)

 
 
1.0 [reference]
11.8 (1.5–92.5)
2.0 (1.1–3.8)
2.1 (1.5–2.9)

1.0 [reference]
1.0 (.7–1.5)
1.0 (.6–1.5)
1.3 (.9–1.8)
1.3 (.9–1.9)
1.4 (1.0–1.9)
.1 (.0–1.2)

1.0 [reference]
1.0 (.7–1.5)
1.0 (.6–1.5)
1.3 (.9–1.8)
1.3 (.9–1.9)
1.4 (1.0–1.9)
.1 (.0–1.2)

1.0 [reference]
3.7 (3.1–4.4)

1.0 [reference]
3.7 (3.1–4.4)

1.0 [reference]
1.5 (1.1–2.2)
2.1 (1.7–2.8)

1.0 [reference]
1.5 (1.1–2.2)
2.2 (1.7–2.8)

1.0 [reference]
1.4 (1.1–1.8)
2.6 (1.9–3.6)
3.3 (2.5–4.3)
3.6 (1.8–7.2)

1.0 [reference]
1.4 (1.1–1.8)
2.5 (1.8–3.5)
3.2 (2.5–4.3)
3.6 (1.8–7.2)

1.0 [reference]
1.8 (1.0–3.1)
1.6 (1.2–2.1)
1.7 (1.3–2.2)
2.2 (1.7–3.0)
2.7 (1.8–3.9)

1.0 [reference]
1.8 (1.0–3.2)
1.6 (1.2–2.1)
1.7 (1.3–2.2)
2.2 (1.7–3.0)
2.7 (1.8–3.9)

on imprisonment reveals the potentially broad
impact of any association between incarceration and
morbidity and mortality.
Mass incarceration disrupts marriage and labor
markets (Huebner 2005; Lopoo and Western 2005;
Pager 2003; Wilson 1987), perpetuates ethnic and
class inequality (Pettit and Western 2004; Western
2002), influences the outcome of national elections

(Uggen and Manza 2002), and places the broader
population at greater risk of infectious diseases
(Stucker et al. 2008). Recent studies provide evidence
that the effects of incarceration extend to negative
health outcomes, revealing individual-level effects of
incarceration on morbidity (Fazel and Baillargeon
2011; Massoglia 2008a, 2008b; Schnittker and John
2007) and mortality (Binswanger et al. 2007; Rosen

224	

Journal of Health and Social Behavior 55(2)

Table 3.  Age-adjusted Odds of Specific Causes of Death by Lifetime Prevalence of Incarceration
(n = 1,741).
Proportion of Deaths
Cause of Death
Cancer
Cerebrovascular diseases
Ischaemic heart disease
Other cardiovascular
Mental disorder
Respiratory disease
Infectious disease
Chronic liver disease +
cirrhosis
Other digestive disease
Drowning
Acute alcohol poisoning
Other accidental
poisoning
Homicide
Suicide
External, cause
undetermined
Transport injuries
Other external causes
All other causes

Ever Incarcerated
(n = 292)

Never Incarcerated
(n = 1,449)

7.2
3.8
11.6
12.0
1.4
11.6
6.8
6.5

10.3
6.1
15.5
12.2
1.0
7.0
2.3
6.8

.75 (.47–1.22)
.70 (.37–1.34)
.85 (.57–1.27)
.96 (.65–1.42)
1.36 (.45–4.14)
1.79 (1.19–2.71)
3.10 (1.74–5.50)
.93 (.56–1.55)

4.1
0.7
3.1
4.1

3.7
1.1
5.9
1.4

1.17 (.61–2.22)
.58 (.13–2.56)
.50 (.25–1.00)
2.32 (1.11–4.87)

4.8
5.5
4.1

2.1
7.2
6.7

1.99 (1.04–3.82)
.68 (.39–1.18)
.53 (.29–.99)

3.1
5.8
3.8

2.3
4.3
4.2

1.24 (.59–2.64)
1.26 (.72–2.19)
.83 (.43–1.61)

et al. 2008; Spaulding et al. 2011) and populationlevel effects of incarceration rates on life expectancy
(Wildeman 2012).
The results of this rigorous large-scale populationbased case-control study of incarceration and premature mortality are clear. Men who had been
incarcerated were more than twice as likely as those
who had not to experience premature mortality.
Relative to decedent males who had never been incarcerated, decedent ex-inmates were significantly more
likely to die from infectious diseases, respiratory diseases, non–alcohol-related accidental poisonings
(usually drug overdoses), and homicide. Considered
alongside other research, these findings reveal not
only that incarceration has immediate and durable
effects on morbidity upon release from prison, but
that its consequences may extend to a greater risk of
early death. Thus, to the list of extralegal sanctions
experienced by those who have been imprisoned, we
add this mortality penalty of incarceration.
The findings presented here are consistent with
results from prior research, not only in terms of

OR (95 percent CI)

incarceration’s effect on negative health outcomes
but also with regard to causes of death and effect
size. Relative to decedents who had not been incarcerated, I found that decedents who had been incarcerated were more likely to die from infectious
diseases, respiratory diseases, non–alcohol-related
accidental poisonings, and homicide. Earlier studies of incarceration and mortality also often found
an excess of deaths from these causes, especially
infectious diseases, drug overdose, and homicide.
The higher risk of death due to infectious and respiratory diseases is consistent with the literature on
greater exposure to infectious diseases while
imprisoned, including HIV, hepatitis C, and tuberculosis (Johnson and Raphael 2009; Massoglia
2008a; Stuckler et al. 2008).
Further, while effect sizes vary between studies,
the ORs estimated here, both for men who had been
incarcerated in the year prior to death (OR = 11.8)
and for men who had been released at least one
year before death (OR = 2.2), are generally similar
to those from earlier studies.

Pridemore	

Implications for Other Health-related
Phenomena
Incarceration and its association with morbidity
and mortality likely have implications and collateral consequences for other health-related phenomena. First, the empirical literature provides
consistent evidence of an association between
criminal offending and premature mortality, especially for chronic and violent offenders, in both
Europe and the United States (Lattimore, Linster,
and MacDonald 1997; Laub and Vaillant 2000;
Paanila, Hakola, and Tiihonen 1999; Piquero et al.
2014; Sattar and Killias 2005). Incarceration, however, is rarely if ever discussed as a contributing
factor. Piquero et al. (2014), for example, relied on
the work of Gottfredson and Hirschi (1990) and
Moffitt (1993) to explain their finding that highrate chronic offenders experience excess mortality.
Laub and Vaillant (2000:96) suggested and tested
four competing hypotheses—risk taking and
impulsiveness, substance use, poor self-care, and
economic and educational deprivation—but found
only modest support and concluded that “[a]
lthough delinquency is strongly associated with
premature mortality, the etiological links remain
unclear.” Incarceration is absent from these discussions but may provide a partial explanation, especially since the association between offending and
early death is stronger among those most likely to
come into contact with the penal system (i.e.,
chronic, high-rate, and violent offenders) and since
offenders are more likely to die from infectious
diseases.
Second, not only are ex-inmates a vulnerable
population, but they can serve as vectors for disease and other health problems, and thus the negative health consequences of imprisonment extend
beyond the incarcerated to family members, communities, and the public. Partners and children of
incarcerated men suffer higher rates of negative
physical and mental health outcomes (Wildeman,
Schnittker, and Turney 2012), and children of
incarcerated men are also at greater risk of behavioral problems (Wakefield and Wildeman 2011).
Ex-inmates’ partners are at high risk of sexually
transmitted infections (STIs) that the men contracted while in prison. Similarly, there is a positive
association between a neighborhood’s incarceration rate and its prevalence of STIs (Johnson and
Raphael 2009; Thomas and Torrone 2006) and
other negative health outcomes, especially in cities
(Freudenberg 2001). Further, increasing incarceration rates are directly responsible for the growing

225
prevalence of TB and multidrug-resistant TB in
European and Central Asian nations (Stuckler et al.
2008). A similar pattern exists in the United States,
especially with hepatitis C, which spreads to the
public when inmates are released (Weinbaum,
Lyerla, and Margolis 2003). Through these and
other mechanisms, the burden of illness spills over
from prisons and ex-inmates, with important consequences for family, community, and population
health.
The association between incarceration and morbidity and mortality may contribute to other known
health inequalities.6 As Thacher (2004:90) stated in
his study of inequality in crime victimization by
socioeconomic status, “inequality in the distribution of any social burden is of greatest concern
when it exacerbates the inequalities that accumulate in other spheres of life.” The tremendous
expansion of the penal system has had differential
effects by ethnicity (Pettit and Western 2004). For
example, Western and Wildeman (2009) estimated
that about 23 percent of black men born in the first
half of the 1970s could expect to have been incarcerated at some point by the time they were in their
mid-30s. The corresponding estimate for white
men was less than 3 percent. We also know there
are ethnic disparities in morbidity and mortality.
This includes differences in life expectancy, TB,
and HIV, all of which have now been shown to be
associated with incarceration. If blacks are incarcerated at a much higher rate, and if incarceration
has both immediate and enduring effects on morbidity and mortality, then it is plausible that incarceration is partially responsible for ethnic
disparities in health. Johnson and Raphael (2009)
showed, for example, that changes in black incarceration rates are closely linked to changes in AIDS
prevalence among black men and women and that
the black-white racial disparity in AIDS infection
rates during the 1980s and 1990s was almost completely attributable to changes in black incarceration rates during this period. Using state-level
panel data from between 1980 and 2004, Wildeman
(2012) found that incarceration rates were negatively associated with population health. He also
found that the strength of the association was substantial for blacks and that mass imprisonment
likely played a role in (1) diminishing health gains
in blacks over this period and (2) racial differences
in life expectancy. As Thoits (2010) noted in her
review, a key conclusion drawn from the literature
on stress and health is that the unequal distribution
of stress in the general population results in
inequalities in physical well-being. Massoglia

226	
(2008a) contends that incarceration is a powerful
sorting mechanism that acts to unequally distribute
exposure to acute and enduring stressors, thereby
increasing the risk of poor health among those who
have been imprisoned. The penal system is already
recognized as a powerful source of social stratification generally (Wakefield and Uggen 2010), and
Massoglia (2008b:275) concluded that “due primarily to disproportionate rates of incarceration,
the penal system plays a role in perpetuating racial
differences” in health.

Limitations
There are a few main limitations to this study that
must be considered. First, the original instrument
was not designed specifically to examine the association between incarceration and premature mortality, and thus the question about incarceration
was vague. Specifically, it asked, “Had he [i.e., the
decedent or the control] ever been in any kind of
prison?” This question is not precise as to the type
of institution and how long the person was incarcerated. Proxy respondents may have interpreted
this question to mean a variety of things, including
pretrial detention. On the other hand, while there is
considerable heterogeneity in the conditions and
length of confinement experienced by formerly
incarcerated men, prior studies also did not assess
the impact of these characteristics. Further, the lack
of precision in the wording of the question likely
means the mortality odds ratios represent conservative estimates since the question probably captured
not only those who had spent years in prison but
also those who spent lesser time in local jails and
detention centers.
Second, there are two further design limitations
that may lead to underestimating the association
between incarceration and premature mortality.
The controls who had been incarcerated had yet to
reach life expectancy, meaning they could still
experience premature mortality. Additionally, to be
included in the sample, cases had to have been living with at least one other person at the time of
death, and controls had to be living with at least
one other person at the time of their random selection into the control series. This was necessary to
collect information about cases (and thus controls)
via proxy respondents. Evidence shows that previously incarcerated men are more likely to be single
and to have relationship difficulties; therefore, they
may be more likely to live alone and thus more
likely to have been excluded from the IFS sample.
Again, however, both limitations would serve to

Journal of Health and Social Behavior 55(2)
downwardly bias the mortality odds ratios estimated here and thus result in conservative estimates of the association between incarceration and
premature mortality.
Third, this analysis was undertaken using a
male sample, and results may not hold for females.
Similarly, the study used Russian data and thus
may not generalize to other nations. One example
is the high rate in Russia of tuberculosis and multidrug-resistant tuberculosis (MDR TB). In 2005,
Russia had TB incidence and mortality rates of 119
and 22 per 100,000 residents, respectively. These
high rates are driven largely by mass incarceration
in Russia (Stuckler et al. 2008), and MDR TB cases
represent about one-quarter of all treated cases in
Eastern Europe (Euro TB and the National
Coordinators for Tuberculosis in the WHO
European Region 2007). Another example is that
premature mortality due to stress-related heart disease is very high in Russia following the collapse
of the Soviet Union (Leon and Shkolnikov 1998).
This might explain the failure to find a higher proportion of deaths due to heart disease among decedents who had been incarcerated. A similar example
is suicide. Prior research showed elevated rates of
suicide among ex-prisoners relative to the comparison population (Binswanger et al. 2007; Lim et al.
2012; Spaulding et al. 2011). However, Russia’s
suicide rate, and especially its male suicide rate, is
among the highest in the world and increased substantially following the collapse of the Soviet
Union (Pridemore and Spivak 2003). Nevertheless,
my findings are consistent with theory and with
key conclusions drawn from recent research on
incarceration and morbidity in the United States
(Massoglia 2008a, 2008b; Schnittker and John
2007) and from studies of the impact of incarceration on morbidity and mortality in the United States
and elsewhere (Binswanger et al. 2007; Fazel and
Baillargeon 2011; Spaulding et al. 2011).
Fourth, it may be that the effect on premature
mortality of incarceration and of the time since
incarceration varies by age, which could lead to an
over- or underestimate of the mortality odds ratio
based on the two-year timeframe of data collection.
While this may be true, especially since the number
of cases and controls who had been incarcerated
was relatively small, any bias in the estimates
resulting from this is likely minimal for several reasons. First, the sample includes subjects with a
range of ages at which premature mortality
occurred and a range of the number of years since
incarceration, meaning the sample includes those
at greater and lower risk points. Next, the vast

Pridemore	
majority of those who had been incarcerated fell
into one of two groups: 1–5 years or more than 5
years since incarceration. As shown in Table 2, the
risk of premature mortality associated with incarceration is the same for both of these groups.
Additionally, as described in Footnote 4, I carried
out further analyses stratifying cases and controls
by age. The results showed no differences in the
size of the mortality odds ratios for those less than
40 and greater than 40 years of age. Further, the
original IFS design deliberately selected the 25 to
54 male age group because it is a relatively narrow
age range where (in the Russian context) the distribution of mortality outcomes is more or less similar, and selection does not begin markedly until
65 years. Nevertheless, the chance for over- or
underestimation remains, and this potential bias
must be considered.
Finally, while case-control designs provide
many advantages, they are vulnerable to selection
effects. The Izhevsk Family Study was not focused
on this specific question and thus steps were not
taken to minimize the risk of selection bias (e.g.,
there was no way of measuring potential confounders before incarceration occurred).7 However, it is
important to point out that prior research found that
(1) several key childhood correlates of offending,
including IQ and early onset delinquency, were not
related to premature mortality (Laub and Vaillant
2000); (2) no childhood traits predicted both later
offending and physical health (Farrington 1995);
(3) the association between chronic offending and
early death held even after controlling for individual and environmental risk factors from childhood
(Piquero et al. 2014), including substance abuse
and psychiatric diagnoses (Stenbacka et al. 2012);
and (4) the association between incarceration and
morbidity remained after controlling for health
prior to imprisonment (Massoglia 2008a). Still,
selection effects are a threat to the validity of the
results and we cannot rule them out.8

Future Research
These and related findings point to a number of
avenues for future research. First, further theorizing and theory testing is required to determine the
precise pathways through which incarceration
influences morbidity and mortality. While I rely on
exposure to infectious diseases, stress, and disruption of social integration to explain this association,
alternative explanations deserve attention. For
example, criminological theories like Gottfredson
and Hirschi’s (1990) general theory of crime (with

227
its attention on low self-control and analogous
risky behaviors) and Moffitt’s (1993) developmental taxonomy (with a focus on the neuropsychological deficits of life course persistent offenders)
may help explain the poorer health and earlier
death of those who come in contact with the penal
system. Further, there may be other causes of negative health outcomes that are specific to time spent
in prison, including poor nutrition while incarcerated, drug use in prison, and the likelihood of starting smoking in prison for those who did not already
smoke or increasing the amount of smoking in
prison among prior smokers. Second, we should
examine more closely the impact of incarceration
and its association with morbidity and mortality on
the relationship between offending and health;
family, community, and population health; and
health inequalities. The latter seems especially
salient, as disparities in the distribution of incarceration by ethnicity may be driving ethnic health
inequalities, and the mortality penalty of incarceration might even help explain the black-white gap in
life expectancy (Wildeman 2012).
Third, we should test to see if sentence length
conditions the association between incarceration
and health. As with estimating the impact of incarceration, estimating the causal effect of sentence
length is difficult because both it and health outcomes may be endogenous to individual characteristics. As suggested by Wildeman (2011), however,
one way to overcome this limitation is to take
advantage of exogenous variation in sentence
length unrelated to the offender. One such source,
employed by Green and Winik (2010) in their analysis of recidivism, is variation in sentence length
due to the sentencing decisions made by different
judges. Fourth, time since release may have an
effect on risk and type of morbidity and mortality.
Several studies show a highly elevated risk of mortality, especially from drug overdose and suicide, in
the days and weeks immediately following release
from prison (Binswanger et al. 2007; Pratt et al.
2006). Lim et al. (2012) provide similar results for
those released from jails, and the findings presented here, while based on small cell counts, also
show a very high risk of mortality for those who
had been incarcerated at some point in the prior
year.
Fifth, there are likely important moderating and
mediating effects to consider in the relationship
between incarceration and premature mortality. It
seems plausible that education, employment, and
social capital may diminish the strength of this
association. There may also be contextual effects

228	
by facility type (e.g., security level, federal vs. state
prisons, jails vs. prisons). Prison and community
health programs vary in their quality of screening
and care, making it likely that the risk of illness due
to and the mortality penalty of incarceration vary
by penal system. Further, while the association
between incarceration and death due to infectious
disease is likely direct, the association between
incarceration and premature mortality due to other
causes may operate indirectly via imprisonment’s
negative effect on other factors known to influence
health, like employment and family stability. Sixth,
there is of course the necessity of creating research
designs that allow for the estimation of causal
effects (Wildeman 2011). There is now clear evidence of an association between incarceration and
morbidity and mortality, both soon immediately
after release and longer term. However, the designs
of these studies remain vulnerable to spurious and
selection effects.
Finally, this is an area where truly interdisciplinary research teams are required. Epidemiologists
and medical and public health researchers are not
only trained in the methods of studying morbidity
and mortality, but they are also often employed by
or have close relationships with administrative
agencies and even prisons themselves. With a focus
on patterns, proximate risk factors, and harm
reduction, however, their research is often less concerned with the theoretical mechanisms through
which the association operates, leaving potentially
helpful measures and tests of association unexplored. This is a key sphere in which sociologists
can be of benefit, especially given a history of
excellent work in discovering the complex causes
of health inequalities. There is an increasing awareness of the role of social forces in seemingly individual health outcomes (Link and Phelan 1995),
and greater cooperation between disciplines and
recognition of the “genes-to-global culture” and
“social symbiome” approach to health (Pescosolido
et al. 2012) will be fruitful in this area.

Conclusion
The findings from this large-scale population-based
case-control study revealed that men who had been
incarcerated were more than twice as likely to experience early death relative to men who had not been
incarcerated. In other words, a mortality penalty
accompanies incarceration. I identified four causes
of death to which these decedent ex-inmates were
significantly more vulnerable compared to other
decedent men: infectious diseases, respiratory

Journal of Health and Social Behavior 55(2)
diseases, non–alcohol-related accidental poisonings
(usually drug overdoses), and homicide. Although
both incarceration and premature mortality are
endogenous to individual characteristics, the association between them remained after controlling for
several of these important characteristics, including
hazardous alcohol consumption, family status, and
socioeconomic status. While other studies have
shown that the period immediately following release
from prison is a dangerous time for ex-inmates, the
current research design de facto provided for a longer term follow-up, making this study among the
first in the literature to do so. I found not only that
the association between incarceration and negative
health outcomes extends to premature mortality, but
that the causes of death to which ex-inmates are vulnerable several years after release are similar to
those to which they are at risk soon after release.
These causes of death also correspond to the findings from the literature that examines the long-term
effects of incarceration on illness.
An often overlooked aspect of the incarcerationhealth association is that prisons actually provide an
opportunity for screening and treating a population
that is otherwise unlikely or unable to take advantage of community-based health care. In addition to
screening and treatment during incarceration, institutions should work with inmates prior to release on
planning for their short- and long-term health care
needs. This will benefit not only the individual
health of prisoners and former prisoners, but population health as well. Nevertheless, screening, planning, and especially treating inmates are expensive
endeavors, and penal systems and their staff are
already tasked with serving populations and undertaking functions that would be more efficiently,
effectively, and humanely addressed in other, more
appropriate settings.
Given the size of penal systems in nations like
the United States and Russia, and the impact of
incarceration on morbidity and mortality, more
research must be done to better understand if and
how mass imprisonment is related to population
health generally and health inequalities specifically. The causes of health inequalities can be
dynamic and may change over time (Link and
Phelan 1995), and given the growth of penal systems worldwide (and especially in the United
States) in recent decades, Massoglia’s (2008b)
hypothesis that the penal system has become a system of health stratification should be tested thoroughly (Wildeman 2012).
In the United States, resorting to mass imprisonment was a political decision. Careful research

Pridemore	
now shows that many of the extralegal consequences of contact with the penal system—especially the mortality penalty of incarceration—go
well beyond what we think about when we think
about punishment. Excess morbidity and mortality
are inconsistent with the tenets of the main philosophies of punishment—retribution, deterrence, and
rehabilitation—and in fact run counter to their ideals. In light of the collateral consequences of mass
imprisonment to individuals, communities, and
society, the size and the mission of the penal system require fundamental reconsideration. The mortality penalty of incarceration should be part of the
debate.

Acknowledgments
I thank (1) Dave Leon and the IFS team for sharing these
data; (2) Dave Leon for comments on and critiques of earlier drafts of this manuscript; (3) the Centre for Baltic and
East European Studies (CBEES) and the Stockholm
Centre on Health of Societies in Transition (SCOHOST),
both at Södertörn University in Stockholm, which provided support for my sabbatical, during which I carried
out the analyses for and wrote this manuscript; and (4)
members of the Social Psychology, Health, and Life
Course (SHeL) workshop in the Sociology Department at
Indiana University, to whom I presented this research and
who provided critical and helpful feedback.

Funding
The author disclosed receipt of the following financial
support for the research, authorship, and/or publication of
this article: The original Izhevsk Family Study was
funded by the Wellcome Trust.

Notes
1.	

2.	

While I use case-control data collected in Russia,
and while this study is one of the first to address the
topic in that country, it is also one of the few studies
to address the incarceration-mortality association
more generally. Therefore, I focus attention less on
Russia specifically and more on the general association between incarceration and premature mortality.
Social science research in Russia was stunted during the Soviet era and is only beginning to recover.
Thus, there is little research in Russia on the collateral consequences of mass imprisonment at the
population-level or on the individual-level effects
of incarceration (see Bobrik et al. 2005 for a summary of the scant research and data that have been
published). There is little reason to believe, however, that incarceration in Russia is dissimilar to the
United States in terms of these main potential explanations for its effect on morbidity and mortality.
Exposure to infectious diseases while incarcerated

229
is greater in Russia, and having been incarcerated
increases the risk of the development of tuberculosis 6 to 12 times in the country depending upon
place type of incarceration (Coker et al. 2006).
Prior incarceration in Russia also influences social
stigma and employability and sometimes comes
with restrictions on where one can reside.
3.	 Men at a higher risk of unstable relationships are
also at a higher risk of incarceration. For example,
while there is little difference in the prevalence of
fatherhood between incarcerated and non-incarcerated men, the former are much less likely to be
married (see Chapter 6 in Western 2006). Beyond
any selection effect, however, imprisonment can
be harmful to existing relationships and to the formation of stable relationships upon release from
prison.
4.	 Based on a reviewer’s comment, in analyses not
shown here, I stratified by age to explore how the
time reference of the incarceration measure (i.e.,
within prior year, 1–5 years before, more than 5
years before) may bias results. For men in their 40s
and 50s (when most deaths in this sample occurred),
this might produce some variation. Further, a man
in his 50s incarcerated within the prior year may be
different from a man in his 20s incarcerated within
the prior year. As suggested by the reviewer, I stratified the sample into less than 40 years old and more
than 40 years old. I was unable to do this stratified
analysis for those incarcerated within the past year
due to very small cell counts. Among those less than
40 years old, there were only eight cases and one
control who had been incarcerated in the prior year.
Among those more than 40 years old, there were
nine cases and no controls who had been incarcerated in the prior year. I did stratify by age for lifetime prevalence of incarceration. In that case, the
results were almost exactly the same for all groups.
For the full sample: odds ratio (OR) = 2.2, 95 percent confidence interval (CI): 1.6–3.0; for the <40
sample: OR = 2.1, CI: 1.3–3.7; for the >40 sample:
OR = 2.2, CI: 1.5–3.2.
5.	 Massoglia (2008a, 2008b) also found that 5 percent of his subsample of the National Longitudinal
Survey of Youth who were at least 40 years old and
had been administered the “Health 40” module had
been incarcerated.
6.	 The data employed in this analysis were from
Russia and thus cannot be used to make direct inferences about health inequalities by ethnicity in the
United States. However, given the similarity in findings from this study and those from other European
nations and from the United States, there is little
reason to expect major differences in the general
conclusions drawn, nor thus in their implications.
7.	 Similarly, in this study we cannot discern what
proportion of the risk of premature mortality might
be due directly to chronic and/or serious offending
instead of incarceration.

230	
8.	

Journal of Health and Social Behavior 55(2)
Although one way to address selection effects is
propensity score matching (see Massoglia 2008a
for an application to incarceration and health), this
method is inappropriate for case-control designs.
As pointed out by Allen and Satten (2011:52), this
method should be limited to prospective studies
because (a) “exposure probabilities in a case-control study are not representative of the target population, so the estimated propensity score does not
correspond to that in the target population” and (b)
“comparing the difference in proportions of persons
with disease in the exposed and the unexposed (the
typical effect measure for a propensity score analysis) is problematic with case-control sampling,
since the proportion of persons with disease in the
study population is fixed by design.” Månnson
et al. (2007) show that when using propensity score
matching in case-control studies there is the likelihood of artifactual effects on the odds ratios and
(due to the failure of propensity scores to converge
to the true value) a reduction in the ability to control
for confounding factors.

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Author Biography
William Alex Pridemore is Distinguished University
Professor in the Department of Criminal Justice and
Criminology at Georgia State University, where he is also
senior researcher in the cluster on evidence-based policy.

Pridemore	
His main research interests include the impact of social
structure on homicide and suicide rates, the role of alcohol in violence and mortality, the sociology of health and
illness, and rural sociology and criminology. Recent publications appear in American Journal of Public Health,

233
Addiction, British Journal of Sociology, Journal of
Research in Crime and Delinquency, Journal of
Quantitative Criminology, and Social Science Research.
He is the 2012 winner of the Radzinowicz Memorial
Prize from the British Journal of Criminology.